CHRONIC OBSTRUCTIVE PULMONARY DISEASE [COPD] By Dr. Zahoor

Chronic Obstructive Pulmonary Disease (COPD) What is COPD ? A disease state characterized by air flow limitation that is not fully reversible Air flow limitation is usually progressive and associated with inflammatory response of the lung to the noxious particles or gases Two conditions come under the term ‘COPD’ 1. Chronic Bronchitis 2. Emphysema

COPD Epidemiology and Aetiology In developed countries, cigarette smoking accounts for 90% of cases In developing countries, only 10-20% of heavy smokers develop COPD, indicating individual susceptibility COPD is related to the number of cigarette smoked per day Climate and air pollution are lesser causes of COPD

COPD Pathophysiology There is increased number of mucous secreting goblet cells in the bronchial mucosa In advanced cases, bronchi become inflamed and pus is seen in the lumen Microscopically - Chronic inflammatory cells are seen in the wall of bronchi, lymphocyte infiltration CD8+ is seen - Columnar cells are replaced by squamous epithelial cells - Inflammation is followed by scaring and thickening of the wall which causes narrowing of small air ways

Pathological changes in the airways in COPD

COPD COPD includes the diagnosis of 1. Chronic Bronchitis 2. Emphysema Cough with sputum on most days for 3 consecutive months for at least 2 years in a row There is inflammation of bronchi, it causes narrowing of bronchi, cough, wheezing and chest tightness Emphysema Abnormal permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of their walls, without obvious fibrosis

Normal Respiratory Tract

Chronic Bronchitis

Alveoli in healthy lung and in COPD

COPD Types of Emphysema 1. Centri Acinar Emphysema There is distension and damage of lung tissue around respiratory bronchioles, while more distal alveolar ducts and alveoli are well preserved This type of emphysema may cause substantial air flow limitation

COPD Types of Emphysema (cont) 2. Pan Acinar Emphysema This is less common There is distension and destruction of whole acinus, there is bullae formation Ventilation perfusion (VA/Q) mismatch occur Cause α1 – Antitrypsin deficiency 3. Irregular Emphysema There is scarring and damage affecting the lung parenchyma which is patchy

COPD Emphysema Emphysema leads to expiratory air flow limitations and air trapping Loss of lung elastic recoil results in increase TLC (total lung capacity) Loss of alveoli decreases capacity for gas transfer VA/Q ( ventilation/perfusion) mismatch leads to fall in PaO2 and increase work of respiration

COPD Emphysema CO2 excretion is less affected and many patients have low normal PaCO2 values due to increased alveolar ventilation Patients are breathless but rarely cyanosed Heart failure and edema are rare These patient are called Pink Puffers

COPD Chronic Bronchitis Those patients who have hypoxia and CO2 retention (Chronic Bronchitis), they appear less breathless NOTE – Increase in CO2 causes stimulation of respiratory center but in high concentration, it causes depression of respiratory center These patients are often cyanosed, oedematous but not so breathless These patient have peripheral vasodilatation, bounding pulse, coarse flapping tremor of outstretched hands when PCO2 is increased to 10 KPa ( 75mmHg).

COPD Chronic Bronchitis (cont) Due to renal hypoxia, there is increased RBC production (leading to polycythaemia) and fluid retention These patient become bloated, plethoric and cyanosed – typical appearance of Blue Bloater

COPD Chronic Bronchitis If we administer O2 to abolish hypoxaemia, by administering O2, it can make situation worse by decreasing respiratory drive as these patients depend on hypoxia to drive their ventilation

COPD

Pink Puffers (Emphysema) and Blue Bloaters (Chronic Bronchitis) COPD Difference between Pink Puffers (Emphysema) and Blue Bloaters (Chronic Bronchitis) Pink Puffer Blue Bloater Build Thin Obese Cyanosis - + Breathlessness ++ Hyperinflation of chest +++ Cor pulmonale + (often)

COPD Clinical Features of COPD Productive cough with white sputum Wheeze and breathlessness usually after many years of smoker’s cough Cold causes frequent infective exacerbation with purulent sputum Other precipitating factors – foggy weather, atmospheric pollution

COPD Clinical Features ( cont) Systemic effects of COPD include - Hypertension - Osteoporosis - Depression - Weight loss - Reduced muscle mass - General weakness

Pulmonary and Systemic Features of COPD

COPD Signs Wheezes in the chest Tachypnea in severe disease with prolonged expiration Accessory muscles of respiration are used, there may be intercostal indrawing on inspiration and pursing of lips on expiration Chest expansion is poor Lungs are hyper inflated Severe Hypercapnia causes confusion, drowsiness Papilloedema may be present

COPD Respiratory failure In COPD, respiratory failure occurs when there is PaO2 < 8 kPa (60 mmHg) or PaCO2 > 7 kPa (55 mmHg) Chronic alveolar hypoxia and Hypercapnia leads to constriction of pulmonary arterioles and pulmonary hypertension Note: Respiratory failure is type 1 and type 2 Type 1: PaO2 is low & PaCO2 is normal or low Cause : Pneumonia Type 2: PaO2 is low & PaCO2 is high Cause : COPD, Respiratory center depression e.g. drugs

COPD Pulmonary Hypertension (Corpulmonale) What is Corpulmonale ? It is right ventricular hypertrophy (failure) secondary to lung disease (pulmonary hypertension) On examination, patient is centrally cyanosed due to lung disease Left para sternal heave is felt due to right ventricular hypertrophy Loud P2 (Pulmonary second sound) Signs of right ventricular failure (increase JVP, Ascites, liver enlargement, peripheral oedema)

COPD Diagnosis FEV1 is reduced in COPD COPD FEV1 % Mild 70% [60-70%] 70% [60-70%] Moderate 60% [50-60%] Severe < 50% Very severe < 30 %

FEV1 curve Flow volume loop b

COPD Other investigations CO gas transfer factor is low in emphysema X-ray chest – shows signs of hyperinflation of lungs with low flattened diaphragm High resolution CT- scan Hemoglobin and PCV (Packed cell volume) may be increased due to secondary polycythaemia

X-ray Chest COPD

COPD Other investigations (cont) Blood gases show hypoxaemia and Hypercapnia Sputum examination – strept pneumoniae and H.Influenzae produced acute exacerbations ECG – right ventricular hypertrophy, tall P-wave (pulmonary hypertension) Echo cardiography – to assess cardiac function α1 Antitrypsin level

COPD Management Smoking should be stopped Drug therapy – it is used for Short term management of exacerbations and Long term management Bronchodilators – β2 agonist e.g. salbutamol – Anti muscarinic drugs e.g. Ipratropium – Theophyllines – Corticosteroids – Anti biotic – Diuretic therapy – Oxygen therapy

COPD Oxygen Therapy Continuous O2 2L/minute via nasal prongs to achieve O2 saturation of greater than 90% O2 is given 15-19 hours daily at home

COPD Nocturnal Hypoxia COPD patients get severe arterial hypoximia during REM sleep and PaO2 may fall very low 2.5 kPa (19 mmHg) Most COPD death occur at night possibly due to cardiac arrhythmias due to hypoxaemia

COPD Treatment for Nocturnal Hypoxaemia Patient should not be given sleeping tablets as they will depress respiratory drive Give O2 at night and ventilatory support BIPAP – Bi-level Positive Airway Pressure It is non invasive positive pressure ventilation given by tight fitting nasal mask It provides inspiratory and expiratory assistance

COPD Pulmonary Rehabilitation Exercise training e.g. walking Physiotherapy Stop smoking Nutritional advice Vaccine – Pneumococcal, Influenza

COPD Important In Type 2 respiratory failure PaCO2 is elevated and the patient is dependent on hypoxic drive. Therefore, O2 therapy is given with care so that PaCO2 should not rise and pH should not be allowed to fall below 7.25

Thank you